DSLD in warmbloods and crosses

I am so sorry to hear of what you’re going through. Thank you for sharing.

I also echo my concern with judges - the breeding trend that we see right now is going towards bigger, straighter (IMO) horses, who are morphologically well exceeding their skeletal limitations.

The point is, I don’t put very much faith in judges right now, because they are rewarding breeders who are breeding horses like this; look at Fuerstenball, who is very popular as a sire and was very popular as a YH… his soft pasterns never held him back when IMHO they should have.

We’re getting to the point where breeders are breeding for sales or for YH classes, and that is very bad because it’s a perfect ouroboros of bad decision making – because a horse’s conformation as a YH is very different than at 18, or 25 – and it’s important that we breed sound horses, within and without - and I don’t think the AHS, particularly, some major dressage lines, is going in the right direction WRT future soundness of their registry.

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@Libby2563 I am so sorry about your horse. What a tragic course of events on a young, talented, beautiful horse.

I had a horse, a TB, who was incredibly talented and gorgeous but had “soft” hind pasterns from a young age. I knew about this from the PPE but then no one was really talking about DSLD and the vet said he should be fine for an eventing/jumper career. The horse started off on the hot side but developed great for a few years, then got less and less predictable to the point he was downright dangerous to ride/explosive. I noticed a slight increase in pastern dropping over the years, but it was extremely gradual. The horse also presented with behavior consistent with back issues, though he was never sore to palpate which I found weird. And he was the king of getting ulcers every five minutes. I now tend to think that constantly ulcer-prone horses may well have something going on that worries them.

I finally woke up and realized he was a poster child for DSLD when he was 12ish and retired him. I have to wonder now how miserable I was making the poor horse trying to ride him for years when I bet his connective tissues all over were bothering him and causing the increasingly poor behavior in a horse that generally wanted to please.

I think it took me a while to realize all the underlying issues, because he was a gorgeous and talented youngster and could have been the real deal as an eventer so I kept sinking years and money into him. He had the movement for dressage and the heart over fences, and he was going so well there for a while. Horses are such heartbreakers.

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I wonder too if seeing it much more in TBs, or in WBs, or any other breed that isn’t really well-known for it (such as the Pasos), has to do with any popularity of certain bloodlines that sometimes congregate in a given area, often a geography close to a popular stallion. So when it pops up, it’s going to pop up there a lot more than, say, if there’s a popular European stallion that US breeders are using, where offspring are then scattered around.

Since ESPA is the new name to more closely correlate to it being a whole body, systemic issue, and not just related to the suspensory structure, I’d say you are not wrong that it’s because of the disease :frowning:

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Sad/confusing update on my guy.

Dr. Halper at UGA emailed me directly last night to let me know the biopsy was “strongly suggestive of DSLD.” I actually wasn’t expecting that and felt physically sick. I asked some follow-up questions and she then said she was “swayed” by his young age and lameness. That in turn made me ask if the histology itself was inconclusive and she said, “Sorry, it was pretty conclusive after the special stain.”

I am still a bit confused, to be honest. “Strongly suggestive” and “pretty conclusive” don’t sound very scientific to me. Is she cushioning the emotional blow? Or is there some doubt? How good is this test actually? As mentioned in my previous post, excellent vets have varying opinions about its value. I have calls/emails into three of the vets who have seen the horse to ask about interpretation of this result.

I have him scheduled for an MRI next week to investigate his 3.5/5 left front lameness that has only gotten worse over 6 months of rest. Now I don’t know whether that would be throwing good money after bad. He is not insured so it would be $3k out of pocket, for a horse that one vet has directly told me he wouldn’t put any more money into and three other vets have told me is unlikely to ever be a performance horse due to his hind end conformation. The problem is that I don’t have a diagnosis for his left front, which is his limiting issue at the moment, so it is hard to give up on him. If he has a bone bruise or traumatic injury in the left front that could heal, he could still be a nice trail or lower level horse. I don’t want to throw a horse away based on probabilities and incomplete information. May start my own thread to get feedback on this aspect actually…

For those interested, he is a Hanoverian by Bugatti out of a Del Piero mare.

I am so sorry to hear this. :frowning:

I am wondering if the wording she is using is because the nuchal ligament biopsy is still so new for many vets, and requires some personal interpretation of the stain – it’s not like some blood tests we have, where they “test positive” for a specific thing. I do know that they believe a higher incidence of proteoglycan levels within the tissue, and also, abnormal structuring of the decorin in the connective tissue, is indicative of “highly likely to have DSLD”. AKA, when they read the stain and the results, I don’t believe they use language like “Confirmed to have DSLD” - rather, it’s “suggestive, likely, unlikely” since it is not the same as being flagged as positive for a specific substance or disease.

Really sorry to hear that. Do they show the stain to you? They must take a picture of it, or something, to confer with other vets…

Thank you. :frowning: Yes, I think the hedgy language is because it isn’t a clear yes/no test and does require interpretation. The person who interpreted it is Dr. Halper at the University of Georgia, who I believe invented the test. My vet took the sample and sent it to her for analysis. It doesn’t sound as though she has conferred with other vets on the slides themselves, just on the history of the horse.

Even “highly likely” would give me more peace of mind than “suggestive” or “pretty consistent.” Ugh.

I still haven’t seen the report because my vet’s front office didn’t see it in my file, my vet hasn’t called me back, and when I asked Dr. Halper to send it to me directly she said that she already faxed it to my vet yesterday. I’m extremely frustrated right now.

That’s the worst. :frowning: honestly I would read that language as a strong positive. As for the MRI, I don’t think I would do it at this point. I’d be tempted to pull his shoes and put him out for a year and see what you have next spring. So sorry.

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I would think if anyone knows how to read the histology on this it would be Dr. Halper! From what I’ve read, only necropsy is conclusive. So I can see how she might be prone to using other more vague words on biopsy. Perhaps she’s also not great at delivering Dx via email? Very frustrating.

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I would ask Dr. Halper for the terminology used for rating/grading the tissue. There should be a standardized scale of rating the severity. I was an editor reading anatomic pathology reports for years and our industry has a standardized scale of description that all pathologists refer to (i.e., mild = X, moderate = Y, severe = Z). If you can get those definitions and then the actual written report from Dr. Halper, that should help you interpret the results.

Maybe before you do the MRI, see if you can do a bute trial or gabapentin and determine if you are able to relieve your horse’s pain and improve the quality of life. If there is not a significant enough response to the pain relief or if it doesn’t help the LF lameness, you might reconsider doing any additional diagnostics like the MRI. At that point, I’d move to full retirement until quality of life degrades or consider euthanasia.

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I have a 16 yr old Oldenburg mare who was diagnosed last August with possible DSLD based on bilateral presentation of suspensory branch desmitis; three of which were well enlarged, also the fiber pattern. Vet flexed, palpated and ultrasounded. This mare has a long (read expensive) history of medical issues, mostly unrelated to her legs. Based on the above I chose to retire her.

HERE is the QUESTION: Twice in the last month, she has had incidents where her stifle has locked. As I was thinking about this I got to wondering: IF she has DLSD could this stifle situation be related? Has anyone else seen this? Same leg as the worst of the two suspensory ultrasounds.

FYI, her breeding is: sire - Iroquois who goes back to Inschallah and Diamont on his dam’s side. Dam of my mare goes quickly back to Donnerhall and Grundstein, with a thoroughbred or two tossed in.

If the failing suspensories are causing the stifle to straighten then yes, it could be related. But as a by-product, not as a direct correlation. In other words, UFP is not related to DSLD, but can be a symptom of a straightening hind leg.

Thanks JB, that is helpful.

But DSLD affects all soft tissue, which would include the stabilizing structure of the stifle, so why could locking stifle (if a horse does not have a history of it) be related to DSLD?

UFP has 2 general root causes. The ligament is too tight, and once in the locked position, has a tough time getting over the hook. Or, it’s too loose, and inappropriately gets hooked over the ligament such that the position of the leg is not conducive to actively unhooking it.

That’s why estrogen injections don’t always help - that helps loose ligaments (think about how foaling (or our birthing) requires hips to open up - as if the issue is the ligament is already too loose… And that’s why the ligament splitting doesn’t always work, as the goal there is to effectively lengthen the ligament.

Ok, 3 causes - the quadriceps and associated muscles are weak, and don’t do a good job activating the joints to unhook the ligament.

I suppose it could be kindasorta possible, hadn’t thought about it, that ESPA would “stretch” that patellar ligament such that it ends up in the 2nd cause of UFP above. Maybe it does contribute. But we know that when ESPA progresses enough, the hocks straighten, the stifle straightens, and a straight(er) stifle is well-known to be a contributing factor in UFP

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